Lazy eye and your child's sight Supersonic powder injection |
|||||||
MALARIA: The old enemy strikes fiercely Look for coconut Lima: A simple biological control technique using coconuts, a fruit that is both cheap and abundant in tropical zones, could become a new treatment for malaria. The disease is endemic in those parts of the world with a humid, tropical climate that provides an abundance of stagnant water where the malaria-carrying mosquitoes breed. Its victims are mostly the inhabitants of the poorest countries, which generally lack basic sanitation services. Malaria kills three million people annually, nearly double the present number of victims succumbing to AIDS (Acquired Immune Deficiency Syndrome), according to the World Health Organisation (WHO). In Africa alone, it kills one million children each year while in Latin America, 1% of the population of Peru is infected with malaria. The disease is transmitted by the Anopheles mosquito, which can live at altitudes of up to 3,000 metres and whose bite injects the plasmodium parasite into the human body. It can cause death within 72 hours if treatment is not provided in time. The majority of people in malaria zones have the parasite in their bodies, that is, they live with the parasite almost continuously. They go to health centres when they become feverish to receive medicine but, when they feel better, they stop taking it, says Luis Valdez, a specialist in infectious diseases. As a consequence, the malaria parasite becomes drug-resistant, allowing pregnant women to transmit the parasite to their foetuses. In addition, even if a person completes the quinine-based treatment course, they can then be bitten again by a mosquito and re-infected, adds the expert. For these reasons, the best way to attack the disease is through prevention. One of the traditional methods is to spray the marshes where the mosquitoes breed with insecticide, but the chemicals are expensive and generally toxic to both humans and the environment. Now, the Peruvian microbiologist Palmira Ventosilla, of the Institute of Tropical Medicine of the private Cayetano Heredia University of Lima, has developed a biological control method that uses coconuts to grow a micro-organism which in turn kills the anopheles larvae, but does not harm other living things or the environment. This micro-organism is produced commercially in industrialised countries, but its importation is too expensive for poor countries afflicted by the disease. For a long time, Ventosilla searched for a simple method to naturally develop this bacillus, known by its scientific name of Bti, and finally found what she was looking for in coconuts, a fruit that grows abundantly in tropical zones. A small quantity of Bti is introduced into the coconut through a hole that is then plugged with cotton and sealed with candle wax. The hard shell of the coconut protects the incubating bacillus, and the milk inside contains amino acids and carbohydrates necessary for its reproduction, Ventosilla explains. After two or three days of fermentation, the coconuts are taken to the swamps where the mosquitoes live, the plugs are removed and the coconuts are thrown into the stagnant pools of water. Two or three coconuts are enough to cover a typical pond. Experiments have demonstrated that this quantity kills all the larvae contained in the marshy pond, and keeps working for 45 days. In reality, the reproduction of Bti is not a problem. The harder job is to win over the local people to accept this technique as one that is viable and effective, says Ventosilla. She began her experiments in Salitral, a semi-tropical zone on the northern Peruvian coast where marshes abound, as does the mosquito that transmits the disease. Its population consists mostly of peasants with a minimal level of education and it was very difficult to convince them to abandon the use of insecticides and adopt the coconut treatment. It was also easy for the locals to wait for the periodic inoculations provided by the Ministry of Health and to simply go to health centres every time they ran a high fever, and experienced intense chills and sweating. Now, three years after the treatments effectiveness was put to the test during the El Nino phenomenon - which had prompted authorities to fear a major outbreak of the disease across the whole northern Peruvian coast - the population is enthusiastically participating in training sessions. They bring their own knives and candle wax and seem very interested in learning the right way to soak the cotton with Bti, to insert into the coconut, says one of the instructors on Ventosillas multi-disciplinary team, composed of biologists, entomologists, sociologists and anthropologists. A fundamental factor in the acceptance of this alternative technique was the children. Jorge Velez, one of the team members, devised a way to teach them about the life-cycle of the mosquito and how to make Bti using coconuts. The children then became the biggest advocates of biological control to their parents. With assistance from the International Centre on Research and Development (ICRD) of Canada, Ventosillas team is ready to start a second round in villages of the department of Madre de Dios, in the southern Peruvian Amazon. The goal
is to prove the hypothesis that overhead vegetation and
algae protect the Bti bacillus from damage caused by the
suns ultraviolet rays, a factor that could be
important for the future refinement and expansion of the
malaria-control programme. |
Pill and will on test Malaria is still afflicting a vast number of people in India and the neighbouring countries. Its eradication remains elusive even as newer antimalarial drugs both branded and generic (unbranded) have been flooding the medicine market. We decided to put 17 brands of the commonest antimalarial drug, chloroquine phosphate, to the test and find out how effective or otherwise they were. And unlike our earlier test reports, we found the costliest generic product topping the quality chart. We tested five national brands which occupy more than 60 per cent of the total marketshare. They had a uniform price, but differed in quality. So did the three regional brands. But the nine generic formulations showed considerable variations in price and quality. Genesis On August 20, 1897, in a small laboratory in Hyderabad, Sir Ronald Ross discovered the malarial parasite in a dissected Anopheles mosquito. This discovery helped millions of people to escape a malaria-linked death. The building at Begumpet is still a silent monument to this great benefactor of mankind. The association of malaria with 'evil (bad) air' (from which the term arises) and marshlands was ascertained even in the days of Hippocrates. No wonder, malaria came to be known also as marsh fever. An effective treatment with the cinchona bark and its active ingredient, quinine, had been used universally since 1700. But it was only in the beginning of the twentieth century that the exact roles of mosquitoes and malarial parasites were known. Chloroquine was synthesised in 1934, and provided an effective and affordable drug for treating malaria. Chloroquine Phosphate tablets are now sold as an over-the-counter (OTC) drug. Brands tested We tested 17 brands of chloroquine phosphate tablets (national and regional brands as well as generic tablets) purchased from around the country. These brands from the maximum chunk of the market size. Five of them are national brands: Cloquin, Emquin, Lariago, Nivaquine-P and Resochin. Of the 12 regional products, three are branded: Leoquin EC, Malariaquin and Welquin. The remaining nine are generic chloroquine phosphate tablets. All except the generic product from Lark Laboratories were of 250 mg. Lark was labelled as 500 mg. The tablets were a mix of different categories such as: uncoated, sugar-coated, film coated and enteric coated. The brands were tested against specifications laid down in the Indian Pharmacopoeia (IP). How effective? The test
for dissolution is a critical parameter in determining
the performance and defining the quality of tablets and
capsules. It measures the actual amount of drug released
in the gastro-intestinal fluid and made available to the
body. Dissolution, therefore, has been given significant
weightage in our rating. Dissolution has been
incorporated in the IP since December, 1996. |
Lazy eye and
your child's sight The eye of a newborn baby functions from day one but the vision develops in the first month of the life as the use increases. Vision continues to develop up to six years if the eyes and the brain develop normally. Any condition which interferes with the use of the eyes during this period can lead to the decreased development of vision. Lazy eye is poor vision in an otherwise structurally normal eye that did not develop normal sight during early childhood. It is also called "Amblyopia". In spite of the structurally normal eye, the image on the retina is not being interpreted because there has been some interference in the development of vision during childhood. It usually affects one eye but sometimes it may affect both eyes too. About 1 to 3 per cent of the pre-school and school-age children have lazy eye. It can be treated only if diagnosed during infancy or early childhood. So, parents must be aware of this condition if they want their child to see properly in later life. Poor vision is usually the only symptom of lazy eye. There is no pain or redness associated with it. A child may not be aware of having one good eye and one poor eye. Quite often, poor vision in one eye is detected very late when the child by chance happens to cover the good eye. Squint (misaligned eyes) is the most common cause of lazy eye. Nearly 50% of the children with squint have lazy eye. For normal development of vision, the child should have normal alignment of both eyes during the first six years of life. If squint occurs during this age, the normal vision will not develop and the child will have reduced vision in the squinting eye. Also, when one eye squints, two different images are sent to the brain. The brain will recognise the image of the straight eye and ignore the image of the squinting eye to avoid double vision. This causes the loss of depth perception Lazy eye may also occur when one eye is out of focus because it is more nearsighted, farsighted or astigmatic than the other eye. Whenever there is a difference of 2.0 D or more in the power of glasses in the two eyes, the eye with the higher power of glasses becomes lazy. Light stimulates the development of vision in children. Any condition that prevents the entry of light into the eye interferes with the development of vision. The upper eyelid covering more than half of the eye by birth or due to any swelling, cloudiness in the front transparent window (cornea) of the eye and the lens in a child interferes with the entry of light into the eye and will lead to lazy eye. Lazy eye is detected by finding a difference in vision between each eye. It is easy to detect poor vision in school-going age by asking the child to read the vision chart. However, it is difficult to detect poor vision in infant and pre-school age children. Some observations help to detect poor vision in these young children. Watch how well the child follows objects with each eye when the other eye is covered. The child will have difficulty in following objects if the good eye is covered. Watch the behaviour of the child when one eye is covered. If one eye has poor vision and the good eye is covered, the child may try to remove the cover or may start crying. If he has squint only in one eye at all times, it indicates poor vision in that eye. If the child squints both eyes but one eye squints more frequently than the other, the eye that squints more often has poor vision. If the child has any condition that interferes with the entry of light into the eye, the eye will have poor vision. An eye specialist can detect poor vision even in very young children by using some special tests. It is important to realise that the treatment of the condition that causes lazy eye does not cure the lazy eye. Thus straightening the squinting eye by surgery, correcting the blurred vision with glasses or removing the cloudy cornea or lens do not cure the lazy eye and it is treated separately. To correct lazy eye, the child must be forced to use the lazy eye. This is usually done by closing the good eye with a patch, often for several months. In addition to patching, the child is advised to do near-visual exercises like threading beads, tracing pictures and playing video games. This further forces the use of lazy eye. A readymade patch is available in the market but it is costly. You can make a patch from the roll of a two-inch-wide microspore tape available at a chemists shop. Any occluder that attaches on the spectacles should not be used because the child can remove spectacles along with occluder very easily. The patch should be applied in such a way that it covers the eye completely and should be used for all waking hours. This is called full-time patching. Never keep both eyes open. After removing the patch, apply some cream or moisturiser on the skin so that the skin remains healthy. Remember that if the child uses the patch only occasionally or removes the patch during waking hours, it will not be effective. A continuous patching of the good eye may decrease the vision in the good eye. This is avoided by opening the good eye and patching the lazy eye in between. The eye doctor will tell you for how many days you should patch the good eye and open the lazy eye. Once vision has improved to the maximum or when there is no further improvement in spite of sincerely using the patch for three or four months, full-time patching is stopped and amblyopia is declared untreatable. After stopping full-time patching, part-time patching a (few hours a day) should be done to maintain the improved vision. Vision usually becomes stable by the age of eight or nine years. Thus, a child who has been treated for lazy eye should wear a part-time patch and have his vision check-up every three to six months up to this age. If vision goes down at any time, again a course of full-time patching is needed. Usually, there is very little possibility of vision going back after the age of eight or nine years. Occasionally, lazy eye is treated by blurring the vision of the good eye with special eye drops, but this treatment is much less effective than patching. Similarly, the oral intake of certain drugs has been tried for treating lazy eye but it has not been found better than patching. Remember that glasses do not cure lazy eye in most of the cases. There is no surgical treatment for lazy eye. Also the intake of vitamin A, carrots, good diet, etc, has no role in the treatment of lazy eye. The patching of the good eye to treat lazy eye is most successful when the child is pre-school age. If treatment is delayed, vision loss usually becomes permanent. As a rule, the earlier amblyopia is detected and treated, the better is the visual results. An eye specialist can instruct parents about how to treat amblyopia, but it is the responsibility of the parents to carry out this treatment. No child likes to have a patch on the good eye, but parents must convince their child to do what will be best for him. Successful treatment mostly depends upon parental interest and involvement, and their ability to gain their child's cooperation. They must understand that the treatment of lazy eye requires a lot of patience. They should not expect miracles. It takes several months and requires repeated visits to the eye doctor to assess the result of treatment. A half-hearted and irregular treatment generally leads to disappointment. If lazy eye is not treated in time, it will develop permanent vision loss and the child will be unfit for several occupations. Also, if the vision in the good eye is lost later in life due to an accident or a disease, life-long dependence on others results. Lazy eye, therefore, must be detected and treated as early as possible. The
author is the chief of the Squint and Amblyopia Clinic
and Associate Professor of Ophthalmology at the PGI,
Chandigarh. |
Supersonic powder injection Delivering medication through the skin efficiently without using conventional needles has been one of the medical industry's longest quests. Several patented devices developed over the past 50 years have not been widely adopted because of inherent disadvantages in some of the delivery mechanisms. In May 1993, robotics engineer Paul Drayson teamed up with Brian Bellhouse -- the inventor of a new delivery system -- to set up PowderJect Limited in Oxford, southern England, to develop a technique to turn drugs and vaccines into powder and then shoot them into the skin. This method differs significantly from Intraject, another needle-less injector designed by United Kingdom inventor Terry Weston and marketed by Weston Medical of Richmond, southern England. Intraject's technique involves the use of a pre-filled, disposable injector which forces very fine, high-pressure jets of air to force liquid vaccine under the skin. The principle underlying PowderJect's technology is that particles of solid-form drugs can be painlessly delivered into the body at high efficiency travelling at a high velocity. These drugs may be therapeutic agents or vaccines and may be small molecules, peptides, proteins or genes. The technique can be applied using the appropriate injection system to deliver any drug formulated as a solid particle of the appropriate size, mass, density and strength through the skin, the tissues of the mouth and other routes. When the delivery mechanism is activated, the PowderJect system opens a gas canister which allows helium gas at high pressure to enter a chamber at the end of which is a drug cassette containing the powdered drug between two plastic membranes. At the designed release pressure, virtually instantaneous rupture of both membranes causes the gas to expand rapidly, forming a strong shock wave which travels down the nozzle at speeds of 600-900 metres per second. Behind this shock wave is the initial gas flow which carries the drug particles, accelerating them to a speed approaching 750 metres per second. As the shock wave, followed by the helium gas containing the drug particle, leaves the nozzle and hits the skin surface, the drug particles have sufficient momentum to penetrate the skin while the helium gas is reflected into a silencer. Individual tiny particles of drug powder pass through the outer layer of the skin tracking down to the required level of penetration in the tissue. The drug dissolves and then either acts locally or diffuses into the bloodstream to deliver its therapeutic effect. Initially, PowderJect is focusing on delivery through the skin and the mouth but it also intends to develop systems for delivery by means of a catheter to internal organs and for delivery directly into the eye. Mr Drayson said of the system: "It offers a much more gentle form of injection. As well as being needle-free and painless, it avoids the risk of needle-stick injury and, more importantly, it shoots the medication to a precise layer of skin, in some instances improving the efficacy of the treatment." PowderJect Vaccine Incorporated a wholly owned subsidiary of PowderJect Pharmaceuticals Plc, focuses on the application of the PowderJect technology to the administration of DNA (deoxyribonucleic acid) matter and conventional vaccines. The company, which has branches in California and Wisconsin in the United States, is developing other products for the prevention and treatment of a broad range of infectious diseases and cancer. Additional vaccine applications include auto-immune diseases, allergies and other immunopathologies. Other products in development based on its proprietary system in several important fields, include local anaesthesia, erectile dysfunction, migraine, osteoporosis and diabetes. BCN (For
further information, contact: PowderJect Pharma-ceuticals
Plc, 4 Robinson Avenue, Oxford, U.K.) |
| . |